Bo-Yi Yang1, Shujun Fan2, Elisabeth Thiering3, Jochen Seissler4, Dennis Nowak5, Guang-Hui Dong6, Joachim Heinrich7. 1. Guangzhou Key Laboratory of Environmental Pollution and Health Risk Assessment, Guangdong Provincial Engineering Technology Research Center of Environmental and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, 510080, China; Institute and Clinic for Occupational, Social and Environmental Medicine, Hospital of the Ludwig-Maximilian University Munich, LMU Munich, Member, German Center for Lung Research (DZL Munich), CPC (Comprehensive Pneumology Center Munich), Germany; Institute of Epidemiology, Helmholtz Zentrum München- German Research Center for Environmental Health, Neuherberg, Germany. 2. Guangzhou Center for Disease Control and Prevention, Guangzhu, 510440, China. 3. Institute of Epidemiology, Helmholtz Zentrum München- German Research Center for Environmental Health, Neuherberg, Germany; Division of Metabolic and Nutritional Medicine, Dr. von Hauner Children's Hospital, University of Munich Medical Center, Munich, Germany. 4. Diabetes Center, Medizinische Klinik und Poliklinik IV - Campus Innenstadt, Ludwig-Maximilians-University, Munich, Germany; Clinical Cooperation Group Type 2 Diabetes, Helmholtz Zentrum München, Neuherberg, Germany. 5. Institute and Clinic for Occupational, Social and Environmental Medicine, Hospital of the Ludwig-Maximilian University Munich, LMU Munich, Member, German Center for Lung Research (DZL Munich), CPC (Comprehensive Pneumology Center Munich), Germany. 6. Guangzhou Key Laboratory of Environmental Pollution and Health Risk Assessment, Guangdong Provincial Engineering Technology Research Center of Environmental and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, 510080, China. 7. Institute and Clinic for Occupational, Social and Environmental Medicine, Hospital of the Ludwig-Maximilian University Munich, LMU Munich, Member, German Center for Lung Research (DZL Munich), CPC (Comprehensive Pneumology Center Munich), Germany; Allergy and Lung Health Unit, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, Australia. Electronic address: Joachim.Heinrich@med.uni-muenchen.de.
Abstract
BACKGROUND: Air pollutants are suggested to be related to type 2 diabetes (T2D). Since several high quality papers on air pollutants and T2D have been published beyond the last reviews, an extended systematic review is highly warranted. We review epidemiological studies to quantify the association between air pollutants and T2D, and to answer if diabetes patients are more vulnerable to air pollutants. METHODS: We systematically reviewed the databases of PubMed and Web of Science based on the guidelines of the Preferred Reporting Items for Systematic review and Meta-analysis (PRISMA). We calculated odds ratios (OR) or hazard ratios (HR) and their 95% confidence intervals (CI) to assess the strength of the associations between air pollutants [e.g., particulate matter with diameter ≤ 2.5 μm (PM2.5), particulate matter with diameter ≤ 10 μm (PM10), and nitrogen dioxide (NO2)] and T2D. We evaluated the quality and risk of bias of the included studies and graded the credibility of the pooled evidence using several recommended tools. We also performed sensitivity analysis, meta-regression analysis, and publication bias test. RESULTS: Out of 716 articles identified, 86 were used for this review and meta-analysis. Meta-analyses showed significant associations of PM2.5 with T2D incidence (11 studies; HR = 1.10, 95% CI = 1.04-1.17 per 10 μg/m3 increment; I2 = 74.4%) and prevalence (11 studies; OR = 1.08; 95% CI = 1.04-1.12 per 10 μg/m3 increment; I2 = 84.3%), of PM10 with T2D prevalence (6 studies; OR = 1.10; 95% CI = 1.03-1.17 per 10 μg/m3 increment; I2 = 89.5%) and incidence (6 studies; HR = 1.11; 95% CI = 1.00-1.22 per μg/m3 increment; I2 = 70.6%), and of NO2 with T2D prevalence (11 studies; OR = 1.07; 95% CI = 1.04-1.11 per 10 μg/m3 increment; I2 = 91.1%). The majority of studies on glucose-homoeostasis markers also showed increased risks with higher air pollutants levels, but the studies were too heterogeneous for meta-analysis. Overall, patients with diabetes might be more vulnerable to PM. CONCLUSIONS: Recent publications strengthened the evidence for adverse effects of ambient air pollutants exposure (especially for PM) on T2D and that diabetic patients might be more vulnerable to air pollutants exposure.
BACKGROUND: Air pollutants are suggested to be related to type 2 diabetes (T2D). Since several high quality papers on air pollutants and T2D have been published beyond the last reviews, an extended systematic review is highly warranted. We review epidemiological studies to quantify the association between air pollutants and T2D, and to answer if diabetespatients are more vulnerable to air pollutants. METHODS: We systematically reviewed the databases of PubMed and Web of Science based on the guidelines of the Preferred Reporting Items for Systematic review and Meta-analysis (PRISMA). We calculated odds ratios (OR) or hazard ratios (HR) and their 95% confidence intervals (CI) to assess the strength of the associations between air pollutants [e.g., particulate matter with diameter ≤ 2.5 μm (PM2.5), particulate matter with diameter ≤ 10 μm (PM10), and nitrogen dioxide (NO2)] and T2D. We evaluated the quality and risk of bias of the included studies and graded the credibility of the pooled evidence using several recommended tools. We also performed sensitivity analysis, meta-regression analysis, and publication bias test. RESULTS: Out of 716 articles identified, 86 were used for this review and meta-analysis. Meta-analyses showed significant associations of PM2.5 with T2D incidence (11 studies; HR = 1.10, 95% CI = 1.04-1.17 per 10 μg/m3 increment; I2 = 74.4%) and prevalence (11 studies; OR = 1.08; 95% CI = 1.04-1.12 per 10 μg/m3 increment; I2 = 84.3%), of PM10 with T2D prevalence (6 studies; OR = 1.10; 95% CI = 1.03-1.17 per 10 μg/m3 increment; I2 = 89.5%) and incidence (6 studies; HR = 1.11; 95% CI = 1.00-1.22 per μg/m3 increment; I2 = 70.6%), and of NO2 with T2D prevalence (11 studies; OR = 1.07; 95% CI = 1.04-1.11 per 10 μg/m3 increment; I2 = 91.1%). The majority of studies on glucose-homoeostasis markers also showed increased risks with higher air pollutants levels, but the studies were too heterogeneous for meta-analysis. Overall, patients with diabetes might be more vulnerable to PM. CONCLUSIONS: Recent publications strengthened the evidence for adverse effects of ambient air pollutants exposure (especially for PM) on T2D and that diabeticpatients might be more vulnerable to air pollutants exposure.
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